Gene interactions and pathways from curated databases and text-mining

◀ Back to NFKB1

NFKB1 — SYK

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Takada et al., J Biol Chem 2003 : First, H2O2 activated Syk in KBM-5 cells ; second, H2O2 failed to activate NF-kappaB in cells that do not express Syk protein ; third, overexpression of Syk increased H2O2 induced NF-kappaB activation ; and fourth, reduction of Syk transcription using small interfering RNA inhibited H2O2 induced NF-kappaB activation
Takada et al., J Immunol 2004 : Jurkat cells that did not express Syk ( JCaM1, JCaM1/lck ) showed lack of TNF induced Syk , JNK, p38 MAPK, and p44/p42 MAPK activation, as well as TNF induced IkappaBalpha phosphorylation, IkappaBalpha degradation, and NF-kappaB activation ... TNF induced NF-kappaB activation was enhanced by overexpression of Syk by Syk-cDNA and suppressed when Syk expression was down-regulated by expression of Syk-small interfering RNA ( siRNA-Syk ) ... The apoptotic effects of TNF were reduced by up-regulation of NF-kappaB by Syk-cDNA , and enhanced by down-regulation of NF-kappaB by siRNA-Syk ... Overall, our results demonstrate that Syk activation plays an essential role in TNF induced activation of JNK, p38 MAPK, p44/p42 MAPK, NF-kappaB , and apoptosis
Ulanova et al., Biochem Biophys Res Commun 2006 : Inhibition of Syk down-regulated TNF induced p38 and p44/42 MAPK phosphorylation and nuclear translocation of p65 NF-kappaB
Gallagher et al., J Neurosci 2007 : CNTF induced SYK phosphorylation is rapidly followed by increased tyrosine phosphorylation of IkappaB-alpha, and blocking SYK activation or tyrosine phosphorylation of IkappaB-alpha prevents CNTF induced NF-kappaB activation and CNTF promoted neurite growth
Oh et al., J Biol Chem 2007 : Inhibition of the activity of Syk prior to, concomitant with or shortly following receptor engagement led to the rapid inhibition of receptor mediated tyrosine phosphorylation and blocked the activation of extracellular signal regulated kinase, NF-kappaB , and NFAT ... The receptor mediated activation of NF-kappaB required active Syk for a relatively short period of time, whereas the activation of NFAT required active kinase for a prolonged ( > 1 h ) period
Bijli et al., J Biol Chem 2008 : Consistent with this, thrombin induced NF-kappaB activity and ICAM-1 expression were prevented by the expression of a kinase-defective mutant or RNA interference knockdown of Syk ... Analysis of the NF-kappaB pathway showed that Syk contributes to thrombin induced NF-kappaB activation by controlling its transactivation potential and that this response is associated with tyrosine phosphorylation of RelA/p65
Bi et al., J Biol Chem 2010 : The scaffold protein CARD9 plays an essential role in anti-fungus immunity and is implicated in mediating Dectin-1/Syk induced NF-kappaB activation in response to Candida albicans infection ... Finally, we find that although both CARD9 and Syk are required for Hyphae induced NF-kappaB activation, they regulate different signaling events in which CARD9 mediates IkappaBalpha kinase ubiquitination, whereas Syk regulates IkappaBalpha kinase phosphorylation